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目的:研究及分析动脉粥样硬化患者外周血单核细胞差异表达基因，筛选动脉粥样硬化潜在的分子标志物。方法:通过GEO数据库获取GSE23746和GSE9820基因芯片数据集。GSE23746包含了76例就诊于华盛顿大学附属医院的颈动脉粥样硬化患者及19例对照者的单核细胞样本。GSE9820包含了18例就诊于荷兰阿姆斯特丹自由大学医学中心的重度病变的冠心病患者及13例对照者的单核细胞样本。分别筛选颈动脉粥样硬化患者及冠状动脉粥样硬化患者相对于对照组的差异表达基因，并确定两个数据集的共同差异表达基因。然后对差异表达基因进行基因本体（GO）及京都基因与基因组百科全书（KEGG）信号通路富集分析。再对差异表达基因进行蛋白相互作用网络（PPI）分析，并选出关键基因。结果:在颈动脉粥样硬化和冠状动脉粥样硬化患者的外周血单核细胞中分别筛选出16个和153个下调的差异表达基因。颈动脉粥样硬化的差异表达基因主要参与炎症反应、中性粒细胞趋化、免疫应答等生物过程；富集到的KEGG通路包括Toll样受体信号通路、NF-κB信号通路、NOD样受体信号通路。冠状动脉粥样硬化的差异表达基因主要参与的生物过程包括核小体装配、凝血、基因表达的调控；富集到的KEGG通路包括系统性红斑狼疮以及细胞因子趋化通路。通过构建PPI网络，在颈动脉粥样硬化患者中识别出5个枢纽基因TNF、IL1B、趋化因子（C-X-C基序）配体8（CXCL8）、趋化因子（C-C基序）配体4（CCL4）、B细胞κ轻肽基因增强子核因子抑制因子（NFKBIA），在冠状动脉粥样硬化患者中识别出5个枢纽基因（组蛋白HIST1H2AC、HIST1H2BJ、HIST1H2BH、HIST2H2AC、HIST2H2BE），这些基因主要参与炎症反应及炎症信号分子的转录和表达。同时还筛选出两个数据集的共同差异表达基因早期生长反应基因1（EGR1）和趋化性细胞因子配体CCL3样蛋白1（CCL3L1）。结论:基于GEO数据库的生物信息学分析，动脉粥样硬化患者外周血单核细胞的炎症信号被抑制；共同差异表达基因EGR1和CCL3L1可作为潜在的生物标志物用于动脉粥样硬化的筛查。这为动脉粥样硬化的机制研究和临床诊疗提供新的思路。“,”Objective:To investigate the differentially expressed genes (DEGs) in circulating monocytes in patients with atherosclerosis (AS) and to identify potential biomarkers for screening AS.Methods:Two gene-chip datasets GSE23746 and GSE9820 were downloaded from the GEO database. The dataset GSE23746 included peripheral monocyte samples from 76 subjects with carotid artery atherosclerosis and 19 controls registered to Washington University hospitals. The dataset GSE9820 included peripheral monocyte samples from 18 patients with atherosclerotic coronary artery disease and 13 controls registered to Vrije Universiteit Medical Center in Amsterdam, the Netherlands. With reference to the controls, the DEGs in patients with carotid artery atherosclerosis and those with coronary atherosclerosis were screened, and the co-differentially expressed genes (co-DEGs) of the two datasets were also identified. The DEGs were then subjected to gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. A protein protein interaction (PPI) network analysis on the DEGs was further performed.Results:A total of 16 and 153 down-regulated DEGs were identified in circulating monocytes from the patients with carotid atherosclerosis and those with coronary atherosclerosis, respectively. The DEGs in patients with carotid atherosclerosis were mainly involved in biological processes such as inflammatory response, neutrophil chemotaxis and immune response; the enriched KEGG pathways of these DEGs included toll-like receptor signaling pathway, NF-κB signaling pathway and NOD-like receptor signaling pathway. The DEGs in patients with coronary atherosclerosis were mainly involved in biological processes such as nucleosome assembly, blood coagulation and regulation of gene expression; the enriched KEGG pathways included systemic lupus erythematosus and chemokine signaling pathway. By constructing a PPI network, five hub genes, namely the TNF, IL1B, CXC-motif ligand 8 (chemokine CXCL8) , CC-motif ligand 4 (chemokine CCL4) , and NF-kappa-B inhibitor alpha (NFKBIA) , were identified in carotid atherosclerosis patients; another five hub genes (histones HIST1H2AC, HIST1H2BJ, HIST1H2BH, HIST2H2AC, and HIST2H2BE) were identified in patients with coronary atherosclerosis. These genes mainly participate in the inflammatory response, and transcription and expression of inflammatory signal molecules. Two co-DEGs[early growth response gene 1 (EGR1) , chemotactic cytokine ligand CCL3-like protein 1 (CCL3L1) ] of the two datasets were also screened.Conclusion:Bioinformatics analysis of GEO database demonstrates the inhibition of inflammatory signals in circulating monocytes in atherosclerotic patients. Co-differentially expressed genes EGR1 and CCL3L1 can be used as potential biomarkers for screening of atherosclerosis. This provides new ideas for mechanistic study, clinical diagnosis and treatment of atherosclerosis.